Centriole Biogenesis Disruption Impairs Regenerative Patterning in Planarians

Abstract

Centrioles are classically known for their role in mitotic spindle formation, yet their broader function in complex tissue regeneration remains poorly defined. Using the planarian Schmidtea mediterranea as a model, this review synthesizes findings from recent studies employing targeted RNAi and pharmacological inhibition to disrupt centriole biogenesis during pharyngeal regeneration. The analysis reveals that centrioles are indispensable, multi-functional organelles governing a hierarchical cascade of regenerative events. Complete inhibition of centriole duplication (e.g., via Plk4 or SAS-6 knockdown) abolishes neoblast proliferation, preventing blastema formation. Partial impairment of centriolar function (e.g., via CEP120 or Centrin knockdown), which spares proliferation, uncovers critical non-mitotic roles. These include directing cell migration via primary cilia-dependent morphogen signaling (e.g., Wnt, Hedgehog) and orchestrating the cytoskeletal remodeling necessary for epithelial polarization and lumenogenesis. Consequently, pharyngeal regeneration fails due to ectopic patterning, tissue disorganization, and functional non-integration. We propose a model wherein centrioles act as central integrators, sequentially ensuring proliferative expansion, spatial coordination, and morphogenetic execution. These findings elevate centrioles from passive structural components to active regulators of regenerative patterning and suggest that centriolar competence may be a critical, yet overlooked, determinant of stem cell efficacy in regenerative contexts.